In Olmsted County, data acquired during the initial cycle of RO1 HL59205 document diverging CHD secular trends as a function of sex and age with less favorable changes in CHD mortality, MI incidence and post-MI mortality and morbidity among the elderly. These data, consistent across all indicators measured, underscore that, notwithstanding the decline in age- adjusted CHD deaths, the burden of CHD remains considerable and the morbidity of MI is substantial despite therapeutic progress. These adverse trends have profound implications in an aging population and their continued monitoring is of paramount importance to understand the burden of CHD. To this end, the clinical criteria to diagnose MI, an essential indicator of CHD, recently changed to rely on troponin, a new biomarker with enhanced diagnostic yield. This will increase the number of cases and shift the spectrum of disease, which has profound clinical as well as public health consequences. Surveillance studies play a central role in the measurement of CHD trends and the interpretation of the epidemiological and clinical implications of such changes, which to date have not been studied. For non-concurrent programs, however this important task poses considerable challenges recognized by the NHLBI Working Group on Community Surveillance, which recommended studies collecting simultaneously troponin and CK/CKMB. Building on methods developed during the initial cycle of our grant, the present competitive renewal proposes a novel active surveillance approach required for the dual ascertainment of each case with both troponin and CK/CKMB. Novel approaches to the procurement of carefully timed blood samples will allow us to directly measure the increase in the number of cases of MI due to troponin, directly ascertain the subsequent change in case mix and interpret outcomes, while also assessing concomitant trends in therapies. Further, we propose to capitalize on this active system to examine the prognostic value of quantitative peak troponin (measured at 24-36 hours) and high sensitivity (hs) CRP (measured early after symptom onset) in our MI cohort. These markers were proposed to stratify risk among cases of acute coronary syndromes with elevated troponin but negative CK/CKMB, classified as MIs by the new criteria, such that prognostic studies should examine jointly the value of both markers. To these ends, we propose four specific aims. 1) To examine the impact of the use of troponin on the incidence of hospitalized MI and test the hypothesis that troponin is temporally associated with an increase in incidence, which has not changed when measured with CK/CKMB 2) To measure the trends in the clinical presentation and severity of MI and test the hypotheses that MIs identified only by troponin are less severe than those identified by CK/CKMB. 3): To study the outcomes of MI and test the hypotheses that, they differ in MIs identified only by troponin as compared to MIs identified by CK/CKMB. 4) To examine the prognostic value of peak troponin and hsCRP to test the hypotheses that they provide prognostic information, incremental to conventional risk indicators. The significance of this study resides in the fact that, through our approach, we will quantify any increase in MI incidence due to troponin, measure directly the resulting change in case mix and analyze subsequent outcomes while simultaneously ensuring continuity for MI surveillance. This is crucial to understand the implications of MI diagnoses as newly defined and changing CHD trends, both aspects critically needed for clinical care as well as for epidemiological studies.